Recent studies have examined: 1) the interaction of enflurane anesthesia and enzyme inducing drugs; 2) whether enflurane, because of its biotransformation to F minus, might be harmful in subjects with renal impairment; and 3) factors influencing anesthetic defluorination unrelated to enzyme induction. Regarding the latter point, Fischer 344 rats were exposed to various length and concentrations of either enflurane or methoxyflurane anesthesia. Proportionally greatest metabolism occurred at the lowest concentration x time of subanesthetic administration and the shortest duration of anesthetic exposure. Regarding enzyme induction in vitro studies with hepatic microsome preparations, in vivo studies in Fischer 344 rats and studies in surgical patients are in agreement. Enchancement of enflurane defluorination does not occur with cytochrome P-450 and P-448 stimulating compounds. However, enflurane defluorination was enhanced after treatment with the antituberculus chemotherapeutic agent, isoniazid. This probably occurs because isoniazid stimulates formation of a cytochrome P-450 variant, cytochrome P-451. Finally, studies in Fischer 344 rats with surgical induced chronic renal impairment indicate that neither enflurane nor halothane exacerbates abnormalities in renal function. Although, serum F minus levels immediately following enflurane anesthesia were highest in animals with impaired renal function, levels 24 hour after anesthesia were the same in all groups and below the nephrotoxic range.